Key clinical point: Leukemic stem cells (LSCs) persisted in bone marrow (BM) but not in peripheral blood (PB) of patients with chronic-phase chronic myeloid leukemia (CML-CP) with deep molecular response (DMR). Investigating BM LSCs before deciding tyrosine kinase inhibitor (TKI) discontinuation could help achieve and maintain stable treatment-free remission (TFR).

Major finding: LSCs persisted in BM of patients in DMR (281.1 LSC/10⁶ white blood cells [WBCs]) but not in PB. BM LSCs were observed in newly diagnosed patients (805 LSCs/10⁶ WBC) and TKI-treated patients with BCR-ABL-positive hematopoiesis (143.5 LSCs/10⁶ WBC). PB LSCs were highest in newly diagnosed patients (237.5 LSCs/μL) but reduced in TKI-treated patients with BCR-ABL-positive hematopoiesis (13.5 LSCs/μL).

Study details: This study included 38 patients with CML-CP who were either recently diagnosed (n=7), had BCR-ABL-positive hematopoiesis under TKI therapy (n=19), or achieved DMR with TKIs (n=12).

Disclosures: This study was funded by Pfizer through Pfizer Independent Medical Grants program. The authors declared no conflicts of interest.

Source: Ilhan O et al. Int J Lab Haematol. 2021 Apr 9. doi: 10.1111/ijlh.13528.

Key clinical point: Leukemic stem cells (LSCs) persisted in bone marrow (BM) but not in peripheral blood (PB) of patients with chronic-phase chronic myeloid leukemia (CML-CP) with deep molecular response (DMR). Investigating BM LSCs before deciding tyrosine kinase inhibitor (TKI) discontinuation could help achieve and maintain stable treatment-free remission (TFR).

Major finding: LSCs persisted in BM of patients in DMR (281.1 LSC/10⁶ white blood cells [WBCs]) but not in PB. BM LSCs were observed in newly diagnosed patients (805 LSCs/10⁶ WBC) and TKI-treated patients with BCR-ABL-positive hematopoiesis (143.5 LSCs/10⁶ WBC). PB LSCs were highest in newly diagnosed patients (237.5 LSCs/μL) but reduced in TKI-treated patients with BCR-ABL-positive hematopoiesis (13.5 LSCs/μL).

Study details: This study included 38 patients with CML-CP who were either recently diagnosed (n=7), had BCR-ABL-positive hematopoiesis under TKI therapy (n=19), or achieved DMR with TKIs (n=12).

Disclosures: This study was funded by Pfizer through Pfizer Independent Medical Grants program. The authors declared no conflicts of interest.

Source: Ilhan O et al. Int J Lab Haematol. 2021 Apr 9. doi: 10.1111/ijlh.13528.

Key clinical point: Leukemic stem cells (LSCs) persisted in bone marrow (BM) but not in peripheral blood (PB) of patients with chronic-phase chronic myeloid leukemia (CML-CP) with deep molecular response (DMR). Investigating BM LSCs before deciding tyrosine kinase inhibitor (TKI) discontinuation could help achieve and maintain stable treatment-free remission (TFR).

Major finding: LSCs persisted in BM of patients in DMR (281.1 LSC/10⁶ white blood cells [WBCs]) but not in PB. BM LSCs were observed in newly diagnosed patients (805 LSCs/10⁶ WBC) and TKI-treated patients with BCR-ABL-positive hematopoiesis (143.5 LSCs/10⁶ WBC). PB LSCs were highest in newly diagnosed patients (237.5 LSCs/μL) but reduced in TKI-treated patients with BCR-ABL-positive hematopoiesis (13.5 LSCs/μL).

Study details: This study included 38 patients with CML-CP who were either recently diagnosed (n=7), had BCR-ABL-positive hematopoiesis under TKI therapy (n=19), or achieved DMR with TKIs (n=12).

Disclosures: This study was funded by Pfizer through Pfizer Independent Medical Grants program. The authors declared no conflicts of interest.

Source: Ilhan O et al. Int J Lab Haematol. 2021 Apr 9. doi: 10.1111/ijlh.13528.

Key clinical point: Tyrosine kinase inhibitor (TKI) discontinuation in patients with chronic-phase chronic myeloid leukemia (CML-CP) is common in routine clinical practice and is as successful as when performed within a clinical trial.

Major finding: TKI discontinuation of longer than 1 month was reported in 235 patients. Overall, 128 patients discontinued as they achieved a deep molecular response, of which 70.3% discontinued outside a clinical trial. Among patients discontinuing TKI outside a clinical trial, 62.2% remained treatment free after a median follow-up of 1.6 years, which compares favorably to that observed in clinical trials.

Study details: This was a retrospective, population-based study of 584 patients diagnosed with CML-CP between 2007 and 2012 from the Swedish CML registry.

Disclosures: No funding source was identified. U Olsson-Stromberg reported honoraria from Ariad. The other authors had no disclosures.

Source: Flygt H et al. Br J Haematol. 2021 Mar 30. doi: 10.1111/bjh.17392.

Key clinical point: Tyrosine kinase inhibitor (TKI) discontinuation in patients with chronic-phase chronic myeloid leukemia (CML-CP) is common in routine clinical practice and is as successful as when performed within a clinical trial.

Major finding: TKI discontinuation of longer than 1 month was reported in 235 patients. Overall, 128 patients discontinued as they achieved a deep molecular response, of which 70.3% discontinued outside a clinical trial. Among patients discontinuing TKI outside a clinical trial, 62.2% remained treatment free after a median follow-up of 1.6 years, which compares favorably to that observed in clinical trials.

Study details: This was a retrospective, population-based study of 584 patients diagnosed with CML-CP between 2007 and 2012 from the Swedish CML registry.

Disclosures: No funding source was identified. U Olsson-Stromberg reported honoraria from Ariad. The other authors had no disclosures.

Source: Flygt H et al. Br J Haematol. 2021 Mar 30. doi: 10.1111/bjh.17392.

Key clinical point: Tyrosine kinase inhibitor (TKI) discontinuation in patients with chronic-phase chronic myeloid leukemia (CML-CP) is common in routine clinical practice and is as successful as when performed within a clinical trial.

Major finding: TKI discontinuation of longer than 1 month was reported in 235 patients. Overall, 128 patients discontinued as they achieved a deep molecular response, of which 70.3% discontinued outside a clinical trial. Among patients discontinuing TKI outside a clinical trial, 62.2% remained treatment free after a median follow-up of 1.6 years, which compares favorably to that observed in clinical trials.

Study details: This was a retrospective, population-based study of 584 patients diagnosed with CML-CP between 2007 and 2012 from the Swedish CML registry.

Disclosures: No funding source was identified. U Olsson-Stromberg reported honoraria from Ariad. The other authors had no disclosures.

Source: Flygt H et al. Br J Haematol. 2021 Mar 30. doi: 10.1111/bjh.17392.

Key clinical point: Upfront imatinib treatment was equally effective in elderly vs. younger patients with chronic myeloid leukemia (CML). Management of therapy-related adverse events (AEs) may lead to better clinical outcomes.

Major finding: Although overall survival was higher in younger patients (P less than .001), rates of early molecular response (MR), complete cytogenic response, major MR, deep MR, and event-free survival were not significantly different between elderly and younger patients. Hematological AEs (24% vs. 7%; P = .005) and AE-related dose reduction (33% vs. 9%; P less than .001) were higher in elderly vs. younger patients.

Study details: Data come from a retrospective study of 158 elderly (aged 60 years or older, n=33) and younger (aged less than 60 years, n=125) patients with Philadelphia-positive CML.

Disclosures: No funding source was identified. The lead author, AE Eşkazan and T Soysal reported ties with various pharmaceutical companies. Other authors declared no conflicts of interest.

Source: Eşkazan AE et al. Clin Lymph Myel Leuk. 2021 Apr 13. doi: 10.1016/j.clml.2021.04.005.

Key clinical point: Upfront imatinib treatment was equally effective in elderly vs. younger patients with chronic myeloid leukemia (CML). Management of therapy-related adverse events (AEs) may lead to better clinical outcomes.

Major finding: Although overall survival was higher in younger patients (P less than .001), rates of early molecular response (MR), complete cytogenic response, major MR, deep MR, and event-free survival were not significantly different between elderly and younger patients. Hematological AEs (24% vs. 7%; P = .005) and AE-related dose reduction (33% vs. 9%; P less than .001) were higher in elderly vs. younger patients.

Study details: Data come from a retrospective study of 158 elderly (aged 60 years or older, n=33) and younger (aged less than 60 years, n=125) patients with Philadelphia-positive CML.

Disclosures: No funding source was identified. The lead author, AE Eşkazan and T Soysal reported ties with various pharmaceutical companies. Other authors declared no conflicts of interest.

Source: Eşkazan AE et al. Clin Lymph Myel Leuk. 2021 Apr 13. doi: 10.1016/j.clml.2021.04.005.

Key clinical point: Upfront imatinib treatment was equally effective in elderly vs. younger patients with chronic myeloid leukemia (CML). Management of therapy-related adverse events (AEs) may lead to better clinical outcomes.

Major finding: Although overall survival was higher in younger patients (P less than .001), rates of early molecular response (MR), complete cytogenic response, major MR, deep MR, and event-free survival were not significantly different between elderly and younger patients. Hematological AEs (24% vs. 7%; P = .005) and AE-related dose reduction (33% vs. 9%; P less than .001) were higher in elderly vs. younger patients.

Study details: Data come from a retrospective study of 158 elderly (aged 60 years or older, n=33) and younger (aged less than 60 years, n=125) patients with Philadelphia-positive CML.

Disclosures: No funding source was identified. The lead author, AE Eşkazan and T Soysal reported ties with various pharmaceutical companies. Other authors declared no conflicts of interest.

Source: Eşkazan AE et al. Clin Lymph Myel Leuk. 2021 Apr 13. doi: 10.1016/j.clml.2021.04.005.

Click here for the Wednesday issue of the SHM Converge Daily News newsletter.

Click here for the Wednesday issue of the SHM Converge Daily News newsletter.

Click here for the Wednesday issue of the SHM Converge Daily News newsletter.

Key clinical point: Bosutinib was more effective than imatinib as first-line treatment of newly diagnosed chronic-phase chronic myeloid leukemia (CML-CP) with manageable toxicity, particularly in the Asian subpopulation of BFORE trial.

Major finding: Rates of major molecular response favored bosutinib vs. imatinib, particularly more in Asian (odds ratio [OR], 2.28; 95% confidence interval [CI], 0.87-5.97) than non-Asian (OR, 1.43; 95% CI, 0.99-2.07) subpopulation. Grade 3/4 treatment-emergent adverse events were more frequent with bosutinib vs. imatinib (72.7% vs. 36.4%) but were manageable.

Study details: This study evaluated 536 patients (Asian, n=67; non-Asian, n=469) with newly diagnosed CML-CP from the phase 3 BFORE trial randomly allocated to either bosutinib or imatinib.

Disclosures: This study was sponsored by Pfizer. The lead author and some of his coinvestigators reported advisory roles, speaker fees, owning stock in, being an employee of, receiving support from, and/or consulting for various pharmaceutical companies, including Pfizer.

Source: Chuah C et al. Int J Hematol. 2021 Apr 13. doi: 10.1007/s12185-021-03144-4.

Key clinical point: Bosutinib was more effective than imatinib as first-line treatment of newly diagnosed chronic-phase chronic myeloid leukemia (CML-CP) with manageable toxicity, particularly in the Asian subpopulation of BFORE trial.

Major finding: Rates of major molecular response favored bosutinib vs. imatinib, particularly more in Asian (odds ratio [OR], 2.28; 95% confidence interval [CI], 0.87-5.97) than non-Asian (OR, 1.43; 95% CI, 0.99-2.07) subpopulation. Grade 3/4 treatment-emergent adverse events were more frequent with bosutinib vs. imatinib (72.7% vs. 36.4%) but were manageable.

Study details: This study evaluated 536 patients (Asian, n=67; non-Asian, n=469) with newly diagnosed CML-CP from the phase 3 BFORE trial randomly allocated to either bosutinib or imatinib.

Disclosures: This study was sponsored by Pfizer. The lead author and some of his coinvestigators reported advisory roles, speaker fees, owning stock in, being an employee of, receiving support from, and/or consulting for various pharmaceutical companies, including Pfizer.

Source: Chuah C et al. Int J Hematol. 2021 Apr 13. doi: 10.1007/s12185-021-03144-4.

Key clinical point: Bosutinib was more effective than imatinib as first-line treatment of newly diagnosed chronic-phase chronic myeloid leukemia (CML-CP) with manageable toxicity, particularly in the Asian subpopulation of BFORE trial.

Major finding: Rates of major molecular response favored bosutinib vs. imatinib, particularly more in Asian (odds ratio [OR], 2.28; 95% confidence interval [CI], 0.87-5.97) than non-Asian (OR, 1.43; 95% CI, 0.99-2.07) subpopulation. Grade 3/4 treatment-emergent adverse events were more frequent with bosutinib vs. imatinib (72.7% vs. 36.4%) but were manageable.

Study details: This study evaluated 536 patients (Asian, n=67; non-Asian, n=469) with newly diagnosed CML-CP from the phase 3 BFORE trial randomly allocated to either bosutinib or imatinib.

Disclosures: This study was sponsored by Pfizer. The lead author and some of his coinvestigators reported advisory roles, speaker fees, owning stock in, being an employee of, receiving support from, and/or consulting for various pharmaceutical companies, including Pfizer.

Source: Chuah C et al. Int J Hematol. 2021 Apr 13. doi: 10.1007/s12185-021-03144-4.

To the Editor:

Levamisole is a veterinary anthelmintic drug with immunomodulating properties that was once approved by the US Food and Drug Administration for the treatment of various conditions, including autoimmune diseases, cancer, pediatric kidney disease, and chronic infections.^1-4 Levamisole was banned in 2000 after reports of associated agranulocytosis and a characteristic painful purpuric vasculitis.^4,5 Despite the ban, its use persists due to its increasing incorporation as an adulterant in cocaine, presumably for its dopaminergic properties that potentiate psychotropic effects.⁶ In 2009, the Drug Enforcement Administration reported that 69% of seized cocaine in the United States contains this chemical, with an average concentration of 10%.⁵ Levamisole-induced vasculopathy (LIV) typically resolves following the cessation of cocaine without further treatment necessary. We present a fatal case of LIV to emphasize that early recognition and discontinuation of the offending agent could be lifesaving.

A 40-year-old woman with a history of cocaine abuse was admitted with tender, reticular, purpuric, and erythematous patches and plaques on the lower extremities with areas of necrosis (Figure 1). The lesions had been present intermittently for 6 months. She tried topical mupirocin and oral amoxicillin clavulanate without improvement. She also described polyarthralgia in the hands, but the remainder of the review of symptoms and physical examination was negative.

The pathogenesis of LIV is not completely understood, but it is thought to be an immune complex–mediated process based on immunofluorescence studies in the skin.^13,14 Classic pathologic findings include multiple fibrin thrombi within small vessels in the superficial and deep dermis, leukocytoclastic vasculitis of small vessels consisting of fibrinoid necrosis of the vessel wall, extravasated erythrocytes, karyorrhectic debris, and angiocentric inflammation.¹⁴ Direct immunofluorescence is not routinely performed but most commonly demonstrates deposition of IgA, IgM, and C3.^14,15

Levamisole-induced vasculopathy usually resolves upon cessation of cocaine use without long-term sequelae. Steroids have been used as treatment of prominent vasculitis with variable success; however, immunosuppressive effects should be closely monitored, especially with inpatients with concurrent granulocytopenia. Broad-spectrum antibiotics have been used in cases with fever and agranulocytosis. Cutaneous lesions typically disappear within 2 to 3 weeks, and serologic markers resolve within 2 to 10 months. Recurrent use of cocaine generally results in recurrent neutropenia and skin eruptions, supporting the causal role. Our patient’s recurrent prolonged cocaine use with vasculopathy was assumed to be the source of the necrotizing fasciitis that led to a cascade of sepsis, rapidly progressing multiorgan failure, and ultimate demise.

Presentation of a purpuric vasculopathy, with or without associated neutropenia and positive autoantibodies, should prompt the consideration of levamisole-contaminated cocaine use in the clinician’s differential. Although the patient may initially deny cocaine use, it is important to keep this diagnosis in mind when the clinical picture fits, and urine toxicology screen should be ordered when there is question. Physicians and patients should be wary of potential complications, even death. Early recognition and discontinuation of the offending agent could be lifesaving.

To the Editor:

Levamisole is a veterinary anthelmintic drug with immunomodulating properties that was once approved by the US Food and Drug Administration for the treatment of various conditions, including autoimmune diseases, cancer, pediatric kidney disease, and chronic infections.^1-4 Levamisole was banned in 2000 after reports of associated agranulocytosis and a characteristic painful purpuric vasculitis.^4,5 Despite the ban, its use persists due to its increasing incorporation as an adulterant in cocaine, presumably for its dopaminergic properties that potentiate psychotropic effects.⁶ In 2009, the Drug Enforcement Administration reported that 69% of seized cocaine in the United States contains this chemical, with an average concentration of 10%.⁵ Levamisole-induced vasculopathy (LIV) typically resolves following the cessation of cocaine without further treatment necessary. We present a fatal case of LIV to emphasize that early recognition and discontinuation of the offending agent could be lifesaving.

A 40-year-old woman with a history of cocaine abuse was admitted with tender, reticular, purpuric, and erythematous patches and plaques on the lower extremities with areas of necrosis (Figure 1). The lesions had been present intermittently for 6 months. She tried topical mupirocin and oral amoxicillin clavulanate without improvement. She also described polyarthralgia in the hands, but the remainder of the review of symptoms and physical examination was negative.

The pathogenesis of LIV is not completely understood, but it is thought to be an immune complex–mediated process based on immunofluorescence studies in the skin.^13,14 Classic pathologic findings include multiple fibrin thrombi within small vessels in the superficial and deep dermis, leukocytoclastic vasculitis of small vessels consisting of fibrinoid necrosis of the vessel wall, extravasated erythrocytes, karyorrhectic debris, and angiocentric inflammation.¹⁴ Direct immunofluorescence is not routinely performed but most commonly demonstrates deposition of IgA, IgM, and C3.^14,15

Levamisole-induced vasculopathy usually resolves upon cessation of cocaine use without long-term sequelae. Steroids have been used as treatment of prominent vasculitis with variable success; however, immunosuppressive effects should be closely monitored, especially with inpatients with concurrent granulocytopenia. Broad-spectrum antibiotics have been used in cases with fever and agranulocytosis. Cutaneous lesions typically disappear within 2 to 3 weeks, and serologic markers resolve within 2 to 10 months. Recurrent use of cocaine generally results in recurrent neutropenia and skin eruptions, supporting the causal role. Our patient’s recurrent prolonged cocaine use with vasculopathy was assumed to be the source of the necrotizing fasciitis that led to a cascade of sepsis, rapidly progressing multiorgan failure, and ultimate demise.

Presentation of a purpuric vasculopathy, with or without associated neutropenia and positive autoantibodies, should prompt the consideration of levamisole-contaminated cocaine use in the clinician’s differential. Although the patient may initially deny cocaine use, it is important to keep this diagnosis in mind when the clinical picture fits, and urine toxicology screen should be ordered when there is question. Physicians and patients should be wary of potential complications, even death. Early recognition and discontinuation of the offending agent could be lifesaving.

To the Editor:

Levamisole is a veterinary anthelmintic drug with immunomodulating properties that was once approved by the US Food and Drug Administration for the treatment of various conditions, including autoimmune diseases, cancer, pediatric kidney disease, and chronic infections.^1-4 Levamisole was banned in 2000 after reports of associated agranulocytosis and a characteristic painful purpuric vasculitis.^4,5 Despite the ban, its use persists due to its increasing incorporation as an adulterant in cocaine, presumably for its dopaminergic properties that potentiate psychotropic effects.⁶ In 2009, the Drug Enforcement Administration reported that 69% of seized cocaine in the United States contains this chemical, with an average concentration of 10%.⁵ Levamisole-induced vasculopathy (LIV) typically resolves following the cessation of cocaine without further treatment necessary. We present a fatal case of LIV to emphasize that early recognition and discontinuation of the offending agent could be lifesaving.

A 40-year-old woman with a history of cocaine abuse was admitted with tender, reticular, purpuric, and erythematous patches and plaques on the lower extremities with areas of necrosis (Figure 1). The lesions had been present intermittently for 6 months. She tried topical mupirocin and oral amoxicillin clavulanate without improvement. She also described polyarthralgia in the hands, but the remainder of the review of symptoms and physical examination was negative.

The pathogenesis of LIV is not completely understood, but it is thought to be an immune complex–mediated process based on immunofluorescence studies in the skin.^13,14 Classic pathologic findings include multiple fibrin thrombi within small vessels in the superficial and deep dermis, leukocytoclastic vasculitis of small vessels consisting of fibrinoid necrosis of the vessel wall, extravasated erythrocytes, karyorrhectic debris, and angiocentric inflammation.¹⁴ Direct immunofluorescence is not routinely performed but most commonly demonstrates deposition of IgA, IgM, and C3.^14,15

Levamisole-induced vasculopathy usually resolves upon cessation of cocaine use without long-term sequelae. Steroids have been used as treatment of prominent vasculitis with variable success; however, immunosuppressive effects should be closely monitored, especially with inpatients with concurrent granulocytopenia. Broad-spectrum antibiotics have been used in cases with fever and agranulocytosis. Cutaneous lesions typically disappear within 2 to 3 weeks, and serologic markers resolve within 2 to 10 months. Recurrent use of cocaine generally results in recurrent neutropenia and skin eruptions, supporting the causal role. Our patient’s recurrent prolonged cocaine use with vasculopathy was assumed to be the source of the necrotizing fasciitis that led to a cascade of sepsis, rapidly progressing multiorgan failure, and ultimate demise.

Presentation of a purpuric vasculopathy, with or without associated neutropenia and positive autoantibodies, should prompt the consideration of levamisole-contaminated cocaine use in the clinician’s differential. Although the patient may initially deny cocaine use, it is important to keep this diagnosis in mind when the clinical picture fits, and urine toxicology screen should be ordered when there is question. Physicians and patients should be wary of potential complications, even death. Early recognition and discontinuation of the offending agent could be lifesaving.

Words matter. So, hear me when I say: I am Asian. I am American. I am a woman. I am not COVID-19. I did not create this virus. I did not place it in my pocket and bring it to the world, sprinkling it like pixie dust, along each path I’ve crossed.

My words create a story, and not just those of one psychiatrist reaching out to others. It’s the story of how the powerful use of words throughout my life inflicted racism upon me, even when unacknowledged by my conscious self. I share my story to let you know you are not alone in your journey of unwinding the cumulative systemic racist words and actions that might have affected your self-identification and self-love. I hope you channel that renewed sense of discovery to empower you to use your own words to create a positive impact for yourself and others – whether it is for your patients, friends, or community.

Currently, I serve as a physician and an advocate. I lead telehealth and developed software that screens for suicide risk (with support of a digital health grant). I also joined friends to develop a by-clinician, for-clinician telemental health platform.

Outside of my Hippocratic Oath, my mission, at its core, was to destigmatize mental illness through cultivating thoughtful conversations. But I am also so much more; aren’t we all? I am a daughter, a sister, an aunt, a friend, and an American. I am working hard to create a life I love – the embodiment of the American Dream. If you meet me face to face, no curriculum vitae, no email, I’m Vietnamese. However, I am not the color of my skin or the shape of my eyes. I am no more defined by my lingering Vietnamese accent than I am by its Texan counterpart. Yet, throughout my life, my Vietnamese ethnicity has been a marker that others have used to define and objectify me.
 

Trauma emerges on national stage

I never thought it would happen to me, but as a resident physician, one of my most traumatic experiences of abusive power was when Donald Trump was running for president in 2016. He was using words and rhetoric that objectified women by classifying and quantifying their “attractiveness.” This culminated in a scandal surrounding a recording in which he said he would grab women by the $%&#@ ... and had been allowed to do so because he was a celebrity. That episode affected me profoundly, maybe more than most. As a child and adolescent psychiatrist, I knew the impact those words could have on future generations, and, as a woman and an aunt, I was appalled. But then, the effect turned to assault. Words matter.

I was living in New York City and as I made my nightly walk home on the Upper East Side, a man followed me. When I walked up the stairs to my building, he actually grabbed me ... by the $%&#@. He did this with the same casual manner that one might greet a coworker with a high-five. He then turned and walked away, laughing. I was overcome with shock; shocked that I could be so violated and yet thankful that he hadn’t taken any more aggressive liberties. He didn’t run away. He walked out as calmly as he had walked in, despite violating a most private piece of my femininity. And he laughed. As much as it jilted me, angered me, and made me feel demeaned and less-than, I know it’s a blessing that the story ended there; so often attacks against women end so much worse.

I questioned: “Why?” Why would this man do this to me? To anyone? I don’t know the answer, but I do know this: The things we normalize through the words we hear in the world, on the news, and at our dinner tables become action. It happened. This man didn’t skulk off into the alleyway. He didn’t hide. He laughed because he felt entitled. That’s because words matter.

My journey is paved with words that mattered. I was born in Vietnam; my family legally immigrated to the United States when I was 5 years old. Throughout grade school, I began to realize the power of spoken words, especially when I was frequently told to go back to where I came from. Questions flew at me like bullets, and whether innocent or borne of curiosity, were hurtful reminders that, through no choice of my own, I was an unwelcome foreigner. “Where are you from?” ... “No, where are you really, really from?” I felt eyes peering through me when my mother packed for me our culture’s traditional foods for lunch. “Ew, what’s that?” ... “That’s gross it smells.” How I longed for the cloak of a peanut butter and jelly sandwich and blonde hair.

As I approached high school, college, and postgraduate work, the “where are you from?” questions didn’t stop but took on a new connotation, as if I were some exotic pet that men had seen walking down the street. “Ooh, what is that?” While history is riddled with the objectification of women, rarely would any woman expect to have a stranger approach her and objectify her with a statement such as: “I only date girls with breast implants.” For Asian women, however, experiencing verbal objectification has become the norm. Each approach I faced was followed by a story about Asian girlfriends of their past and a request for my phone number that felt more like a demand.

What these men probably meant as flirtation, I internalized as inescapable concerns of whether or not they had true desire to get to know me as a person. I became used to unsolicited words and attention from men who objectified me as an exotic fetish. I tried to pretend it was okay, but why? Objectifying Asian women is racism. Their words remind me, and I still hear them, that America has a long history of hypersexualizing Asian women. These words – at their core – dehumanize Asian women, and as we have seen, lead to violence.

Over the past few weeks, there’s been discourse about the mass shooting in Atlanta. We need to pause and remember that the victims, like us, were human. These women killed in Atlanta had husbands, children, siblings, parents, and communities that they were taken away from, senselessly, based solely on their outward appearance. Whether or not this act was perpetrated by someone with a sexual addiction doesn’t matter. What happened is rooted in the systemic racism that has stereotyped Asian women as sexual objects. The perpetrator targeted a group of people because of the systemic racism ingrained in him, plain and simple.

Everybody, no matter how evolved one’s thinking, is influenced by words. You don’t have to have mental illness or malicious intent to fall for propaganda – that’s what makes it so scary, it works so well. Even among my own friends and family, some of the most compassionate people I know, I’ve heard disparaging remarks against Chinese people, from other Asians, repeating the same rhetoric they’ve seen in American newspapers and Asian media outlets, echoing the former president’s coronavirus references to the “Chinese virus.”

But what makes something systemic? What feeds this virus of hate and gives these practices their longevity? Pointing out problems doesn’t make them go away; we have to cultivate conversation based around solutions. And that’s our next step. What can we do to make a positive impact?

Words have affected my life, and my words have given me power. I encourage others to engage in activities where they too can feel empowered. Since the beginning of the pandemic, I’ve leveraged my leadership position with the American Psychiatric Association’s Caucus of Asian American Psychiatrists and used my words to promote advocacy. I’ve also used my voice to raise national attention to the anti-Asian hate activities. Motivated by my own desire to seek a supportive space with others to reflect on our racial identities, I’ve also launched various free support groups for Asian American and Pacific Islanders (AAPI) professionals and health care providers. I want to feel a sense of connection with others who share my experiences, as I never underestimate the phenomenal force of comforting words from a healing community.

Clinicians need their own space for processing, too. It is vitally important for us to take care of ourselves, because our patients’ words can affect our own mental health. My colleagues are shocked by the amount of AAPI patients who are reaching out to them for care. Most of them have not worked with AAPI patients before, because so many people of AAPI descent do not often seek treatment. Many of our patients are dealing with anxiety surrounding their own health and wellness, coupled with financial uncertainties and social unrest. In particular, AAPI clinicians may start to experience bystander trauma, because, for the first time, they are thinking: “It could have been me.” AAPI clinicians are in a unique situation where they have the extra burden of providing a safe space for processing clients’ trauma while also processing their own. We may have experiences of discrimination or racially motivated assaults and can reexperience this trauma through our work. Before we can help others, we have to do a self-check and reflect on how we are doing and seek our own support.

If you are able to take care of yourself and feel empowered to make a difference, there are many ways to help fight against anti-Asian sentiment, both on a personal and more global scale.

We have to check our biases and those of our family, friends, and colleagues. Everyone, even mental health professionals, has biases and is affected by disinformation. We have to dig deep into our own unconscious biases, reflect on them, and commit to changing the biases around us. Do we, or our families, have unconscious biases against a particular minority group? If so, discuss it. No one is to blame. This is systemic, and no one is at fault. White men are not to be vilified. Conservative Republicans are not our enemy. Each of us is human, with our own flaws that can influence our own conscious and unconscious thoughts and actions. Let’s discuss racial issues with our family and friends. Whenever someone says something hateful or discriminatory toward another ethnic group or racial background, we have to call it out, and help them realize their biases and change them.

If you are able, use your words to write to your elected representatives. Send them a short email, no need to be fancy. For example, you can send a note of support for legislation that is similar to the COVID-19 Hate Crimes Act, which passed the Senate on Thursday, April 22, with 94:1 bipartisan support. This kind of legislation is a step in the right direction, but there is still more we must do to stop anti-Asian biases and hate. There is empowerment and healing through making your own voice heard. I hope that these tragic incidents will lead to impactful policy changes.

The next step in this journey of empowerment is speaking about your lived experiences publicly and promoting the voices of others. I dedicated a section of my social media platforms to amplifying Asian voices, sharing news, and updating my hashtags to support the #StopAsianHate movement. I made it a point to form relationships with other advocates, AAPI mental health professionals and those personally affected by anti-Asian hate. Speaking up and speaking out didn’t take away my worries, but it did remind me that I’m powerful and that I am not alone. I can take action and demand action. I do not have to hide in the shadows but can stand in the light, using my voice like a megaphone to call out injustice and intolerance.

I hope that, for AAPI clinicians who may be affected by these current events, this validates your experiences. You are not alone. This is a reminder to treat yourself with empathy as you would your patients. For others, I hope this helps you to learn the plight of many AAPI community members in this country. Together, we can use words to create better neighborhoods, a better country, and safe spaces for all communities, especially the marginalized. As we know, words matter.

Dr. Vo is a board-certified psychiatrist and is the medical director of telehealth for the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia. She is also a faculty member at the University of Pennsylvania, also in Philadelphia. Dr. Vo conducts digital health research focused on using automation and artificial intelligence for suicide risk screening and connecting patients to mental health care services. She disclosed serving as cofounder of telemental health software, Orchid, that eliminates burdensome administrative tasks so that clinicians can focus on their patients and have time for their loved ones.
 

Words matter. So, hear me when I say: I am Asian. I am American. I am a woman. I am not COVID-19. I did not create this virus. I did not place it in my pocket and bring it to the world, sprinkling it like pixie dust, along each path I’ve crossed.

My words create a story, and not just those of one psychiatrist reaching out to others. It’s the story of how the powerful use of words throughout my life inflicted racism upon me, even when unacknowledged by my conscious self. I share my story to let you know you are not alone in your journey of unwinding the cumulative systemic racist words and actions that might have affected your self-identification and self-love. I hope you channel that renewed sense of discovery to empower you to use your own words to create a positive impact for yourself and others – whether it is for your patients, friends, or community.

Currently, I serve as a physician and an advocate. I lead telehealth and developed software that screens for suicide risk (with support of a digital health grant). I also joined friends to develop a by-clinician, for-clinician telemental health platform.

Outside of my Hippocratic Oath, my mission, at its core, was to destigmatize mental illness through cultivating thoughtful conversations. But I am also so much more; aren’t we all? I am a daughter, a sister, an aunt, a friend, and an American. I am working hard to create a life I love – the embodiment of the American Dream. If you meet me face to face, no curriculum vitae, no email, I’m Vietnamese. However, I am not the color of my skin or the shape of my eyes. I am no more defined by my lingering Vietnamese accent than I am by its Texan counterpart. Yet, throughout my life, my Vietnamese ethnicity has been a marker that others have used to define and objectify me.
 

Trauma emerges on national stage

I never thought it would happen to me, but as a resident physician, one of my most traumatic experiences of abusive power was when Donald Trump was running for president in 2016. He was using words and rhetoric that objectified women by classifying and quantifying their “attractiveness.” This culminated in a scandal surrounding a recording in which he said he would grab women by the $%&#@ ... and had been allowed to do so because he was a celebrity. That episode affected me profoundly, maybe more than most. As a child and adolescent psychiatrist, I knew the impact those words could have on future generations, and, as a woman and an aunt, I was appalled. But then, the effect turned to assault. Words matter.

I was living in New York City and as I made my nightly walk home on the Upper East Side, a man followed me. When I walked up the stairs to my building, he actually grabbed me ... by the $%&#@. He did this with the same casual manner that one might greet a coworker with a high-five. He then turned and walked away, laughing. I was overcome with shock; shocked that I could be so violated and yet thankful that he hadn’t taken any more aggressive liberties. He didn’t run away. He walked out as calmly as he had walked in, despite violating a most private piece of my femininity. And he laughed. As much as it jilted me, angered me, and made me feel demeaned and less-than, I know it’s a blessing that the story ended there; so often attacks against women end so much worse.

I questioned: “Why?” Why would this man do this to me? To anyone? I don’t know the answer, but I do know this: The things we normalize through the words we hear in the world, on the news, and at our dinner tables become action. It happened. This man didn’t skulk off into the alleyway. He didn’t hide. He laughed because he felt entitled. That’s because words matter.

My journey is paved with words that mattered. I was born in Vietnam; my family legally immigrated to the United States when I was 5 years old. Throughout grade school, I began to realize the power of spoken words, especially when I was frequently told to go back to where I came from. Questions flew at me like bullets, and whether innocent or borne of curiosity, were hurtful reminders that, through no choice of my own, I was an unwelcome foreigner. “Where are you from?” ... “No, where are you really, really from?” I felt eyes peering through me when my mother packed for me our culture’s traditional foods for lunch. “Ew, what’s that?” ... “That’s gross it smells.” How I longed for the cloak of a peanut butter and jelly sandwich and blonde hair.

As I approached high school, college, and postgraduate work, the “where are you from?” questions didn’t stop but took on a new connotation, as if I were some exotic pet that men had seen walking down the street. “Ooh, what is that?” While history is riddled with the objectification of women, rarely would any woman expect to have a stranger approach her and objectify her with a statement such as: “I only date girls with breast implants.” For Asian women, however, experiencing verbal objectification has become the norm. Each approach I faced was followed by a story about Asian girlfriends of their past and a request for my phone number that felt more like a demand.

What these men probably meant as flirtation, I internalized as inescapable concerns of whether or not they had true desire to get to know me as a person. I became used to unsolicited words and attention from men who objectified me as an exotic fetish. I tried to pretend it was okay, but why? Objectifying Asian women is racism. Their words remind me, and I still hear them, that America has a long history of hypersexualizing Asian women. These words – at their core – dehumanize Asian women, and as we have seen, lead to violence.

Over the past few weeks, there’s been discourse about the mass shooting in Atlanta. We need to pause and remember that the victims, like us, were human. These women killed in Atlanta had husbands, children, siblings, parents, and communities that they were taken away from, senselessly, based solely on their outward appearance. Whether or not this act was perpetrated by someone with a sexual addiction doesn’t matter. What happened is rooted in the systemic racism that has stereotyped Asian women as sexual objects. The perpetrator targeted a group of people because of the systemic racism ingrained in him, plain and simple.

Everybody, no matter how evolved one’s thinking, is influenced by words. You don’t have to have mental illness or malicious intent to fall for propaganda – that’s what makes it so scary, it works so well. Even among my own friends and family, some of the most compassionate people I know, I’ve heard disparaging remarks against Chinese people, from other Asians, repeating the same rhetoric they’ve seen in American newspapers and Asian media outlets, echoing the former president’s coronavirus references to the “Chinese virus.”

But what makes something systemic? What feeds this virus of hate and gives these practices their longevity? Pointing out problems doesn’t make them go away; we have to cultivate conversation based around solutions. And that’s our next step. What can we do to make a positive impact?

Words have affected my life, and my words have given me power. I encourage others to engage in activities where they too can feel empowered. Since the beginning of the pandemic, I’ve leveraged my leadership position with the American Psychiatric Association’s Caucus of Asian American Psychiatrists and used my words to promote advocacy. I’ve also used my voice to raise national attention to the anti-Asian hate activities. Motivated by my own desire to seek a supportive space with others to reflect on our racial identities, I’ve also launched various free support groups for Asian American and Pacific Islanders (AAPI) professionals and health care providers. I want to feel a sense of connection with others who share my experiences, as I never underestimate the phenomenal force of comforting words from a healing community.

Clinicians need their own space for processing, too. It is vitally important for us to take care of ourselves, because our patients’ words can affect our own mental health. My colleagues are shocked by the amount of AAPI patients who are reaching out to them for care. Most of them have not worked with AAPI patients before, because so many people of AAPI descent do not often seek treatment. Many of our patients are dealing with anxiety surrounding their own health and wellness, coupled with financial uncertainties and social unrest. In particular, AAPI clinicians may start to experience bystander trauma, because, for the first time, they are thinking: “It could have been me.” AAPI clinicians are in a unique situation where they have the extra burden of providing a safe space for processing clients’ trauma while also processing their own. We may have experiences of discrimination or racially motivated assaults and can reexperience this trauma through our work. Before we can help others, we have to do a self-check and reflect on how we are doing and seek our own support.

If you are able to take care of yourself and feel empowered to make a difference, there are many ways to help fight against anti-Asian sentiment, both on a personal and more global scale.

We have to check our biases and those of our family, friends, and colleagues. Everyone, even mental health professionals, has biases and is affected by disinformation. We have to dig deep into our own unconscious biases, reflect on them, and commit to changing the biases around us. Do we, or our families, have unconscious biases against a particular minority group? If so, discuss it. No one is to blame. This is systemic, and no one is at fault. White men are not to be vilified. Conservative Republicans are not our enemy. Each of us is human, with our own flaws that can influence our own conscious and unconscious thoughts and actions. Let’s discuss racial issues with our family and friends. Whenever someone says something hateful or discriminatory toward another ethnic group or racial background, we have to call it out, and help them realize their biases and change them.

If you are able, use your words to write to your elected representatives. Send them a short email, no need to be fancy. For example, you can send a note of support for legislation that is similar to the COVID-19 Hate Crimes Act, which passed the Senate on Thursday, April 22, with 94:1 bipartisan support. This kind of legislation is a step in the right direction, but there is still more we must do to stop anti-Asian biases and hate. There is empowerment and healing through making your own voice heard. I hope that these tragic incidents will lead to impactful policy changes.

The next step in this journey of empowerment is speaking about your lived experiences publicly and promoting the voices of others. I dedicated a section of my social media platforms to amplifying Asian voices, sharing news, and updating my hashtags to support the #StopAsianHate movement. I made it a point to form relationships with other advocates, AAPI mental health professionals and those personally affected by anti-Asian hate. Speaking up and speaking out didn’t take away my worries, but it did remind me that I’m powerful and that I am not alone. I can take action and demand action. I do not have to hide in the shadows but can stand in the light, using my voice like a megaphone to call out injustice and intolerance.

I hope that, for AAPI clinicians who may be affected by these current events, this validates your experiences. You are not alone. This is a reminder to treat yourself with empathy as you would your patients. For others, I hope this helps you to learn the plight of many AAPI community members in this country. Together, we can use words to create better neighborhoods, a better country, and safe spaces for all communities, especially the marginalized. As we know, words matter.

Dr. Vo is a board-certified psychiatrist and is the medical director of telehealth for the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia. She is also a faculty member at the University of Pennsylvania, also in Philadelphia. Dr. Vo conducts digital health research focused on using automation and artificial intelligence for suicide risk screening and connecting patients to mental health care services. She disclosed serving as cofounder of telemental health software, Orchid, that eliminates burdensome administrative tasks so that clinicians can focus on their patients and have time for their loved ones.
 

Words matter. So, hear me when I say: I am Asian. I am American. I am a woman. I am not COVID-19. I did not create this virus. I did not place it in my pocket and bring it to the world, sprinkling it like pixie dust, along each path I’ve crossed.

My words create a story, and not just those of one psychiatrist reaching out to others. It’s the story of how the powerful use of words throughout my life inflicted racism upon me, even when unacknowledged by my conscious self. I share my story to let you know you are not alone in your journey of unwinding the cumulative systemic racist words and actions that might have affected your self-identification and self-love. I hope you channel that renewed sense of discovery to empower you to use your own words to create a positive impact for yourself and others – whether it is for your patients, friends, or community.

Currently, I serve as a physician and an advocate. I lead telehealth and developed software that screens for suicide risk (with support of a digital health grant). I also joined friends to develop a by-clinician, for-clinician telemental health platform.

Outside of my Hippocratic Oath, my mission, at its core, was to destigmatize mental illness through cultivating thoughtful conversations. But I am also so much more; aren’t we all? I am a daughter, a sister, an aunt, a friend, and an American. I am working hard to create a life I love – the embodiment of the American Dream. If you meet me face to face, no curriculum vitae, no email, I’m Vietnamese. However, I am not the color of my skin or the shape of my eyes. I am no more defined by my lingering Vietnamese accent than I am by its Texan counterpart. Yet, throughout my life, my Vietnamese ethnicity has been a marker that others have used to define and objectify me.
 

Trauma emerges on national stage

I never thought it would happen to me, but as a resident physician, one of my most traumatic experiences of abusive power was when Donald Trump was running for president in 2016. He was using words and rhetoric that objectified women by classifying and quantifying their “attractiveness.” This culminated in a scandal surrounding a recording in which he said he would grab women by the $%&#@ ... and had been allowed to do so because he was a celebrity. That episode affected me profoundly, maybe more than most. As a child and adolescent psychiatrist, I knew the impact those words could have on future generations, and, as a woman and an aunt, I was appalled. But then, the effect turned to assault. Words matter.

I was living in New York City and as I made my nightly walk home on the Upper East Side, a man followed me. When I walked up the stairs to my building, he actually grabbed me ... by the $%&#@. He did this with the same casual manner that one might greet a coworker with a high-five. He then turned and walked away, laughing. I was overcome with shock; shocked that I could be so violated and yet thankful that he hadn’t taken any more aggressive liberties. He didn’t run away. He walked out as calmly as he had walked in, despite violating a most private piece of my femininity. And he laughed. As much as it jilted me, angered me, and made me feel demeaned and less-than, I know it’s a blessing that the story ended there; so often attacks against women end so much worse.

I questioned: “Why?” Why would this man do this to me? To anyone? I don’t know the answer, but I do know this: The things we normalize through the words we hear in the world, on the news, and at our dinner tables become action. It happened. This man didn’t skulk off into the alleyway. He didn’t hide. He laughed because he felt entitled. That’s because words matter.

My journey is paved with words that mattered. I was born in Vietnam; my family legally immigrated to the United States when I was 5 years old. Throughout grade school, I began to realize the power of spoken words, especially when I was frequently told to go back to where I came from. Questions flew at me like bullets, and whether innocent or borne of curiosity, were hurtful reminders that, through no choice of my own, I was an unwelcome foreigner. “Where are you from?” ... “No, where are you really, really from?” I felt eyes peering through me when my mother packed for me our culture’s traditional foods for lunch. “Ew, what’s that?” ... “That’s gross it smells.” How I longed for the cloak of a peanut butter and jelly sandwich and blonde hair.

As I approached high school, college, and postgraduate work, the “where are you from?” questions didn’t stop but took on a new connotation, as if I were some exotic pet that men had seen walking down the street. “Ooh, what is that?” While history is riddled with the objectification of women, rarely would any woman expect to have a stranger approach her and objectify her with a statement such as: “I only date girls with breast implants.” For Asian women, however, experiencing verbal objectification has become the norm. Each approach I faced was followed by a story about Asian girlfriends of their past and a request for my phone number that felt more like a demand.

What these men probably meant as flirtation, I internalized as inescapable concerns of whether or not they had true desire to get to know me as a person. I became used to unsolicited words and attention from men who objectified me as an exotic fetish. I tried to pretend it was okay, but why? Objectifying Asian women is racism. Their words remind me, and I still hear them, that America has a long history of hypersexualizing Asian women. These words – at their core – dehumanize Asian women, and as we have seen, lead to violence.

Over the past few weeks, there’s been discourse about the mass shooting in Atlanta. We need to pause and remember that the victims, like us, were human. These women killed in Atlanta had husbands, children, siblings, parents, and communities that they were taken away from, senselessly, based solely on their outward appearance. Whether or not this act was perpetrated by someone with a sexual addiction doesn’t matter. What happened is rooted in the systemic racism that has stereotyped Asian women as sexual objects. The perpetrator targeted a group of people because of the systemic racism ingrained in him, plain and simple.

Everybody, no matter how evolved one’s thinking, is influenced by words. You don’t have to have mental illness or malicious intent to fall for propaganda – that’s what makes it so scary, it works so well. Even among my own friends and family, some of the most compassionate people I know, I’ve heard disparaging remarks against Chinese people, from other Asians, repeating the same rhetoric they’ve seen in American newspapers and Asian media outlets, echoing the former president’s coronavirus references to the “Chinese virus.”

But what makes something systemic? What feeds this virus of hate and gives these practices their longevity? Pointing out problems doesn’t make them go away; we have to cultivate conversation based around solutions. And that’s our next step. What can we do to make a positive impact?

Words have affected my life, and my words have given me power. I encourage others to engage in activities where they too can feel empowered. Since the beginning of the pandemic, I’ve leveraged my leadership position with the American Psychiatric Association’s Caucus of Asian American Psychiatrists and used my words to promote advocacy. I’ve also used my voice to raise national attention to the anti-Asian hate activities. Motivated by my own desire to seek a supportive space with others to reflect on our racial identities, I’ve also launched various free support groups for Asian American and Pacific Islanders (AAPI) professionals and health care providers. I want to feel a sense of connection with others who share my experiences, as I never underestimate the phenomenal force of comforting words from a healing community.

Clinicians need their own space for processing, too. It is vitally important for us to take care of ourselves, because our patients’ words can affect our own mental health. My colleagues are shocked by the amount of AAPI patients who are reaching out to them for care. Most of them have not worked with AAPI patients before, because so many people of AAPI descent do not often seek treatment. Many of our patients are dealing with anxiety surrounding their own health and wellness, coupled with financial uncertainties and social unrest. In particular, AAPI clinicians may start to experience bystander trauma, because, for the first time, they are thinking: “It could have been me.” AAPI clinicians are in a unique situation where they have the extra burden of providing a safe space for processing clients’ trauma while also processing their own. We may have experiences of discrimination or racially motivated assaults and can reexperience this trauma through our work. Before we can help others, we have to do a self-check and reflect on how we are doing and seek our own support.

If you are able to take care of yourself and feel empowered to make a difference, there are many ways to help fight against anti-Asian sentiment, both on a personal and more global scale.

We have to check our biases and those of our family, friends, and colleagues. Everyone, even mental health professionals, has biases and is affected by disinformation. We have to dig deep into our own unconscious biases, reflect on them, and commit to changing the biases around us. Do we, or our families, have unconscious biases against a particular minority group? If so, discuss it. No one is to blame. This is systemic, and no one is at fault. White men are not to be vilified. Conservative Republicans are not our enemy. Each of us is human, with our own flaws that can influence our own conscious and unconscious thoughts and actions. Let’s discuss racial issues with our family and friends. Whenever someone says something hateful or discriminatory toward another ethnic group or racial background, we have to call it out, and help them realize their biases and change them.

If you are able, use your words to write to your elected representatives. Send them a short email, no need to be fancy. For example, you can send a note of support for legislation that is similar to the COVID-19 Hate Crimes Act, which passed the Senate on Thursday, April 22, with 94:1 bipartisan support. This kind of legislation is a step in the right direction, but there is still more we must do to stop anti-Asian biases and hate. There is empowerment and healing through making your own voice heard. I hope that these tragic incidents will lead to impactful policy changes.

The next step in this journey of empowerment is speaking about your lived experiences publicly and promoting the voices of others. I dedicated a section of my social media platforms to amplifying Asian voices, sharing news, and updating my hashtags to support the #StopAsianHate movement. I made it a point to form relationships with other advocates, AAPI mental health professionals and those personally affected by anti-Asian hate. Speaking up and speaking out didn’t take away my worries, but it did remind me that I’m powerful and that I am not alone. I can take action and demand action. I do not have to hide in the shadows but can stand in the light, using my voice like a megaphone to call out injustice and intolerance.

I hope that, for AAPI clinicians who may be affected by these current events, this validates your experiences. You are not alone. This is a reminder to treat yourself with empathy as you would your patients. For others, I hope this helps you to learn the plight of many AAPI community members in this country. Together, we can use words to create better neighborhoods, a better country, and safe spaces for all communities, especially the marginalized. As we know, words matter.

Dr. Vo is a board-certified psychiatrist and is the medical director of telehealth for the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia. She is also a faculty member at the University of Pennsylvania, also in Philadelphia. Dr. Vo conducts digital health research focused on using automation and artificial intelligence for suicide risk screening and connecting patients to mental health care services. She disclosed serving as cofounder of telemental health software, Orchid, that eliminates burdensome administrative tasks so that clinicians can focus on their patients and have time for their loved ones.
 

To the Editor:

Cutaneous herpes simplex virus (HSV) infection generally involves mucocutaneous junctions, but virtually any area of the skin can be affected.¹ When the genital area of adult patients is affected, the disease usually is sexually transmitted and mainly caused by HSV-2. In infants, genital primary herpetic infection is rare and more commonly is caused by HSV-1 than by HSV-2. We report a rare case of genital primary herpetic infection with concurrent hepatitis in an infant.

An 8-month-old infant with no underlying medical problems, including atopic dermatitis, was referred for erythematous grouped vesicles with erosions on the perianal area of 4 days’ duration (Figure). The skin color appeared normal, not icterus. She also had a fever (temperature, 37.9 °C), and her urination pattern had changed from normal to frequent leakage, possibly owing to pain related to the eroded lesions. Physical examination did not reveal palpable inguinal lymph nodes. The oral mucosa was not involved. The patient’s father had a history of recurrent herpetic infection on both the perioral and perianal areas.

Although the possibility of systemic involvement including hepatitis due to HSV infection is low, awareness among dermatologists about primary herpetic infection and its possible complications would be helpful in the diagnosis and treatment, especially for atypical or extensive cases.

To the Editor:

Cutaneous herpes simplex virus (HSV) infection generally involves mucocutaneous junctions, but virtually any area of the skin can be affected.¹ When the genital area of adult patients is affected, the disease usually is sexually transmitted and mainly caused by HSV-2. In infants, genital primary herpetic infection is rare and more commonly is caused by HSV-1 than by HSV-2. We report a rare case of genital primary herpetic infection with concurrent hepatitis in an infant.

An 8-month-old infant with no underlying medical problems, including atopic dermatitis, was referred for erythematous grouped vesicles with erosions on the perianal area of 4 days’ duration (Figure). The skin color appeared normal, not icterus. She also had a fever (temperature, 37.9 °C), and her urination pattern had changed from normal to frequent leakage, possibly owing to pain related to the eroded lesions. Physical examination did not reveal palpable inguinal lymph nodes. The oral mucosa was not involved. The patient’s father had a history of recurrent herpetic infection on both the perioral and perianal areas.

Although the possibility of systemic involvement including hepatitis due to HSV infection is low, awareness among dermatologists about primary herpetic infection and its possible complications would be helpful in the diagnosis and treatment, especially for atypical or extensive cases.

To the Editor:

Cutaneous herpes simplex virus (HSV) infection generally involves mucocutaneous junctions, but virtually any area of the skin can be affected.¹ When the genital area of adult patients is affected, the disease usually is sexually transmitted and mainly caused by HSV-2. In infants, genital primary herpetic infection is rare and more commonly is caused by HSV-1 than by HSV-2. We report a rare case of genital primary herpetic infection with concurrent hepatitis in an infant.

An 8-month-old infant with no underlying medical problems, including atopic dermatitis, was referred for erythematous grouped vesicles with erosions on the perianal area of 4 days’ duration (Figure). The skin color appeared normal, not icterus. She also had a fever (temperature, 37.9 °C), and her urination pattern had changed from normal to frequent leakage, possibly owing to pain related to the eroded lesions. Physical examination did not reveal palpable inguinal lymph nodes. The oral mucosa was not involved. The patient’s father had a history of recurrent herpetic infection on both the perioral and perianal areas.

Although the possibility of systemic involvement including hepatitis due to HSV infection is low, awareness among dermatologists about primary herpetic infection and its possible complications would be helpful in the diagnosis and treatment, especially for atypical or extensive cases.

The Diagnosis: Demodicosis 

A clinical diagnosis of facial demodicosis triggered by topical corticosteroid therapy was suspected in our patient. A 3-mm punch biopsy of the right forehead demonstrated a follicular infundibulum rich in Demodex folliculorum with a discrete mononuclear infiltrate in the dermis (Figure 1), confirming the diagnosis. The patient was prescribed metronidazole gel 2% twice daily. Complete clearance of the facial rash was observed at 1-week follow-up (Figure 2). 

Demodex folliculorum is a mite that parasitizes the pilosebaceous follicles of human skin, becoming pathogenic with excessive colonization.^1-3 Facial demodicosis presents as pruritic papules and pustules in a pilosebaceous distribution on the face.^2,3 The diagnosis of facial demodicosis can be difficult due to similarities with many other common facial rashes such as acne, rosacea, contact dermatitis, and folliculitis.  

Similar to facial demodicosis, rosacea can present with erythema, papules, and pustules on the face. Patients with rosacea also have a higher prevalence and degree of Demodex mite infestation.⁴ However, these facial rashes can be differentiated when symptom acuity and personal and family histories are considered. In patients with a long-standing personal and/or family history of erythema, papules, and pustules, the chronicity of disease implies a diagnosis of rosacea. The acute onset of symptomatology and absence of personal or family history of rosacea in our patient favored a diagnosis of demodicosis. 

Pityrosporum folliculitis is an eruption caused by Malassezia furfur, the organism implicated in tinea versicolor. It can present similarly to Demodex folliculitis with follicular papules and pustules on the forehead and back. Features that help to differentiate Pityrosporum folliculitis from Demodex folliculitis include involvement of the upper trunk and onset after antibiotic usage.⁵ Diagnosis of Pityrosporum folliculitis can be confirmed by potassium hydroxide preparation, which demonstrates spaghetti-and-meatball-like hyphae and spores. 

Eosinophilic folliculitis is a chronic sterile folliculitis that usually presents as intensely pruritic papules and pustules on the face with an eruptive onset. There are 3 variants of disease: the classic form (also known as Ofuji disease), immunosuppression-associated disease, and infancy-associated disease.⁶ Eosinophilic folliculitis also may present with annular plaques and peripheral blood eosinophilia, and it is more prevalent in patients of Japanese descent. Differentiation from Demodex folliculitis can be done by histologic examination, which demonstrates spongiosis with exocytosis of eosinophils into the epithelium and a clear deficiency of infiltrating mites.⁶ 

Miliaria, also known as sweat rash, is a common condition that occurs due to occlusion of eccrine sweat glands.⁷ Clinically, miliaria is characterized by erythematous papules ranging from 2 to 4 mm in size that may be vesicular or pustular. Miliaria and demodicosis may have similar clinical presentations; however, several characteristic differences can be noted. Based on the pathophysiology, miliaria will not be folliculocentric, which differs from demodicosis. Additionally, miliaria most commonly occurs in areas of occlusion, such as in skin folds or on the trunk under tight clothing. Miliaria rarely can appear confluent and sunburnlike.⁸ Furthermore, miliaria is less common on the face, while demodicosis almost exclusively is found on the face. 

We present the case of an otherwise healthy patient with acute onset of pruritic papules and pustules involving the superior face following topical corticosteroid use. Similar cases frequently are encountered by dermatologists and require broad differential diagnoses. 

The Diagnosis: Demodicosis 

A clinical diagnosis of facial demodicosis triggered by topical corticosteroid therapy was suspected in our patient. A 3-mm punch biopsy of the right forehead demonstrated a follicular infundibulum rich in Demodex folliculorum with a discrete mononuclear infiltrate in the dermis (Figure 1), confirming the diagnosis. The patient was prescribed metronidazole gel 2% twice daily. Complete clearance of the facial rash was observed at 1-week follow-up (Figure 2). 

Demodex folliculorum is a mite that parasitizes the pilosebaceous follicles of human skin, becoming pathogenic with excessive colonization.^1-3 Facial demodicosis presents as pruritic papules and pustules in a pilosebaceous distribution on the face.^2,3 The diagnosis of facial demodicosis can be difficult due to similarities with many other common facial rashes such as acne, rosacea, contact dermatitis, and folliculitis.  

Similar to facial demodicosis, rosacea can present with erythema, papules, and pustules on the face. Patients with rosacea also have a higher prevalence and degree of Demodex mite infestation.⁴ However, these facial rashes can be differentiated when symptom acuity and personal and family histories are considered. In patients with a long-standing personal and/or family history of erythema, papules, and pustules, the chronicity of disease implies a diagnosis of rosacea. The acute onset of symptomatology and absence of personal or family history of rosacea in our patient favored a diagnosis of demodicosis. 

Pityrosporum folliculitis is an eruption caused by Malassezia furfur, the organism implicated in tinea versicolor. It can present similarly to Demodex folliculitis with follicular papules and pustules on the forehead and back. Features that help to differentiate Pityrosporum folliculitis from Demodex folliculitis include involvement of the upper trunk and onset after antibiotic usage.⁵ Diagnosis of Pityrosporum folliculitis can be confirmed by potassium hydroxide preparation, which demonstrates spaghetti-and-meatball-like hyphae and spores. 

Eosinophilic folliculitis is a chronic sterile folliculitis that usually presents as intensely pruritic papules and pustules on the face with an eruptive onset. There are 3 variants of disease: the classic form (also known as Ofuji disease), immunosuppression-associated disease, and infancy-associated disease.⁶ Eosinophilic folliculitis also may present with annular plaques and peripheral blood eosinophilia, and it is more prevalent in patients of Japanese descent. Differentiation from Demodex folliculitis can be done by histologic examination, which demonstrates spongiosis with exocytosis of eosinophils into the epithelium and a clear deficiency of infiltrating mites.⁶ 

Miliaria, also known as sweat rash, is a common condition that occurs due to occlusion of eccrine sweat glands.⁷ Clinically, miliaria is characterized by erythematous papules ranging from 2 to 4 mm in size that may be vesicular or pustular. Miliaria and demodicosis may have similar clinical presentations; however, several characteristic differences can be noted. Based on the pathophysiology, miliaria will not be folliculocentric, which differs from demodicosis. Additionally, miliaria most commonly occurs in areas of occlusion, such as in skin folds or on the trunk under tight clothing. Miliaria rarely can appear confluent and sunburnlike.⁸ Furthermore, miliaria is less common on the face, while demodicosis almost exclusively is found on the face. 

We present the case of an otherwise healthy patient with acute onset of pruritic papules and pustules involving the superior face following topical corticosteroid use. Similar cases frequently are encountered by dermatologists and require broad differential diagnoses. 

The Diagnosis: Demodicosis 

A clinical diagnosis of facial demodicosis triggered by topical corticosteroid therapy was suspected in our patient. A 3-mm punch biopsy of the right forehead demonstrated a follicular infundibulum rich in Demodex folliculorum with a discrete mononuclear infiltrate in the dermis (Figure 1), confirming the diagnosis. The patient was prescribed metronidazole gel 2% twice daily. Complete clearance of the facial rash was observed at 1-week follow-up (Figure 2). 

Demodex folliculorum is a mite that parasitizes the pilosebaceous follicles of human skin, becoming pathogenic with excessive colonization.^1-3 Facial demodicosis presents as pruritic papules and pustules in a pilosebaceous distribution on the face.^2,3 The diagnosis of facial demodicosis can be difficult due to similarities with many other common facial rashes such as acne, rosacea, contact dermatitis, and folliculitis.  

Similar to facial demodicosis, rosacea can present with erythema, papules, and pustules on the face. Patients with rosacea also have a higher prevalence and degree of Demodex mite infestation.⁴ However, these facial rashes can be differentiated when symptom acuity and personal and family histories are considered. In patients with a long-standing personal and/or family history of erythema, papules, and pustules, the chronicity of disease implies a diagnosis of rosacea. The acute onset of symptomatology and absence of personal or family history of rosacea in our patient favored a diagnosis of demodicosis. 

Pityrosporum folliculitis is an eruption caused by Malassezia furfur, the organism implicated in tinea versicolor. It can present similarly to Demodex folliculitis with follicular papules and pustules on the forehead and back. Features that help to differentiate Pityrosporum folliculitis from Demodex folliculitis include involvement of the upper trunk and onset after antibiotic usage.⁵ Diagnosis of Pityrosporum folliculitis can be confirmed by potassium hydroxide preparation, which demonstrates spaghetti-and-meatball-like hyphae and spores. 

Eosinophilic folliculitis is a chronic sterile folliculitis that usually presents as intensely pruritic papules and pustules on the face with an eruptive onset. There are 3 variants of disease: the classic form (also known as Ofuji disease), immunosuppression-associated disease, and infancy-associated disease.⁶ Eosinophilic folliculitis also may present with annular plaques and peripheral blood eosinophilia, and it is more prevalent in patients of Japanese descent. Differentiation from Demodex folliculitis can be done by histologic examination, which demonstrates spongiosis with exocytosis of eosinophils into the epithelium and a clear deficiency of infiltrating mites.⁶ 

Miliaria, also known as sweat rash, is a common condition that occurs due to occlusion of eccrine sweat glands.⁷ Clinically, miliaria is characterized by erythematous papules ranging from 2 to 4 mm in size that may be vesicular or pustular. Miliaria and demodicosis may have similar clinical presentations; however, several characteristic differences can be noted. Based on the pathophysiology, miliaria will not be folliculocentric, which differs from demodicosis. Additionally, miliaria most commonly occurs in areas of occlusion, such as in skin folds or on the trunk under tight clothing. Miliaria rarely can appear confluent and sunburnlike.⁸ Furthermore, miliaria is less common on the face, while demodicosis almost exclusively is found on the face. 

We present the case of an otherwise healthy patient with acute onset of pruritic papules and pustules involving the superior face following topical corticosteroid use. Similar cases frequently are encountered by dermatologists and require broad differential diagnoses. 

Earlier this spring, Kimberly D. Manning, MD, FACP, FAAP, was caring for an elderly Black man with multiple comorbidities at Grady Memorial Hospital in Atlanta, assembling an order for medications and a discharge plan.

“It was very challenging,” Dr. Manning, professor of medicine and associate vice chair of diversity, equity, and inclusion at Emory University, Atlanta, recalled during a May 4 session at SHM Converge, the annual conference of the Society of Hospital Medicine.

At one point, the patient glanced at her, shrugged, and said: “You know, Doc, we get in where we fit in.”

“He was talking about the idea that people who come from historically disadvantaged backgrounds just have to try to figure it out, have to try to make a dollar out of 15 cents,” Dr. Manning said. “This, to me, really underscores what we mean when we say health disparities, this idea that there are people who are working hard and doing the best that they can but who still are forced to ‘get in where they fit in.’”

The Centers for Disease Control and Prevention defines health disparities as preventable differences in the burden of disease, injury, violence, or opportunities to achieve optimal health that are experienced by socially disadvantaged populations. “When we think about health disparities we often think about many diagnoses,” Dr. Manning continued. “We think about HIV and the disparate care and outcomes we’ve seen in populations of individuals who come from minority backgrounds. We see disparities in obesity, cancer, cardiovascular disease, infant mortality and maternal death, hospital readmissions, and COVID-19. We know that people who do not have access to health care or to healthy neighborhoods and environments or who are economically disadvantaged have poorer outcomes. It plays out with all of these diagnoses.”

In her opinion, health disparities in hospital medicine fall into in one of three buckets: diagnosis and triage, hospital stay and treatment, and sticking the landing – “that is, after a patient leaves the hospital,” Dr. Manning explained. “The hospital stay is the turn on the balance beam. You can do everything perfectly, but then you must dismount. To score a ‘10’ you have to stick the landing. That means being able to get your medications, being able to get to and from clinic appointments, being able to understand the directions you’ve been given. All of these things are intertwined, the inpatient and outpatient care.”

The roots of health disparities in hospitalized patients stem from centuries ago, she said, when America’s health care system was built to benefit white male landowners and their families. Health care for Blacks, on the other hand, “was focused on function, almost like veterinary care, or experimentation,” Dr. Manning said. “After slavery ended, many historically Black institutions of higher learning opened, including medical schools. In 1909, there were seven historically Black medical schools. Acknowledging the history that preceded disparities is essential.”

In her view, the path to improving health care disparities starts with conceding that structural racism exists in the practice of medicine. “This means that health disparities are connected to systemic and individual issues, including our biases,” Dr. Manning said. “Our system was built on this idea that there is greater value of one group of people above others. Access to care, physician workforce, and biases are impacted by system design. Health equity and health equality are not the same.”

She also underscored the importance of the social determinants of health, or “those things we need to be healthy,” including economic stability, neighborhood and physical environment, educational opportunities, access to good food, community and social context, and the idea of health care as a human right and understanding our health care system. “This is what is necessary,” she declared. “Without all of these together, we can’t have the health outcomes that we desire.”

As hospital leaders work to build a more diverse physician workforce, Dr. Manning emphasized the importance of forming antiracism policies by addressing questions such as what will we not stand for? How will we protect and create psychologically safe environments? What is our commitment to diversity in leadership and in trainees? What is our commitment to implicit bias training and bystander training?

“We have to get uncomfortable enough to advocate with urgency because all of these are necessary factors to mitigate health disparities,” she said. “Though the systemic issues are the most urgent, on an individual level, we must continue to disrupt the negative ideology and stereotypes that threaten our environment every day. When we see those negative things, we have to call them out. We need to continue to listen, to humanize those things that are happening around us, and to understand historical context.”

Dr. Manning reported having no financial disclosures.

Earlier this spring, Kimberly D. Manning, MD, FACP, FAAP, was caring for an elderly Black man with multiple comorbidities at Grady Memorial Hospital in Atlanta, assembling an order for medications and a discharge plan.

“It was very challenging,” Dr. Manning, professor of medicine and associate vice chair of diversity, equity, and inclusion at Emory University, Atlanta, recalled during a May 4 session at SHM Converge, the annual conference of the Society of Hospital Medicine.

At one point, the patient glanced at her, shrugged, and said: “You know, Doc, we get in where we fit in.”

“He was talking about the idea that people who come from historically disadvantaged backgrounds just have to try to figure it out, have to try to make a dollar out of 15 cents,” Dr. Manning said. “This, to me, really underscores what we mean when we say health disparities, this idea that there are people who are working hard and doing the best that they can but who still are forced to ‘get in where they fit in.’”

The Centers for Disease Control and Prevention defines health disparities as preventable differences in the burden of disease, injury, violence, or opportunities to achieve optimal health that are experienced by socially disadvantaged populations. “When we think about health disparities we often think about many diagnoses,” Dr. Manning continued. “We think about HIV and the disparate care and outcomes we’ve seen in populations of individuals who come from minority backgrounds. We see disparities in obesity, cancer, cardiovascular disease, infant mortality and maternal death, hospital readmissions, and COVID-19. We know that people who do not have access to health care or to healthy neighborhoods and environments or who are economically disadvantaged have poorer outcomes. It plays out with all of these diagnoses.”

In her opinion, health disparities in hospital medicine fall into in one of three buckets: diagnosis and triage, hospital stay and treatment, and sticking the landing – “that is, after a patient leaves the hospital,” Dr. Manning explained. “The hospital stay is the turn on the balance beam. You can do everything perfectly, but then you must dismount. To score a ‘10’ you have to stick the landing. That means being able to get your medications, being able to get to and from clinic appointments, being able to understand the directions you’ve been given. All of these things are intertwined, the inpatient and outpatient care.”

The roots of health disparities in hospitalized patients stem from centuries ago, she said, when America’s health care system was built to benefit white male landowners and their families. Health care for Blacks, on the other hand, “was focused on function, almost like veterinary care, or experimentation,” Dr. Manning said. “After slavery ended, many historically Black institutions of higher learning opened, including medical schools. In 1909, there were seven historically Black medical schools. Acknowledging the history that preceded disparities is essential.”

In her view, the path to improving health care disparities starts with conceding that structural racism exists in the practice of medicine. “This means that health disparities are connected to systemic and individual issues, including our biases,” Dr. Manning said. “Our system was built on this idea that there is greater value of one group of people above others. Access to care, physician workforce, and biases are impacted by system design. Health equity and health equality are not the same.”

She also underscored the importance of the social determinants of health, or “those things we need to be healthy,” including economic stability, neighborhood and physical environment, educational opportunities, access to good food, community and social context, and the idea of health care as a human right and understanding our health care system. “This is what is necessary,” she declared. “Without all of these together, we can’t have the health outcomes that we desire.”

As hospital leaders work to build a more diverse physician workforce, Dr. Manning emphasized the importance of forming antiracism policies by addressing questions such as what will we not stand for? How will we protect and create psychologically safe environments? What is our commitment to diversity in leadership and in trainees? What is our commitment to implicit bias training and bystander training?

“We have to get uncomfortable enough to advocate with urgency because all of these are necessary factors to mitigate health disparities,” she said. “Though the systemic issues are the most urgent, on an individual level, we must continue to disrupt the negative ideology and stereotypes that threaten our environment every day. When we see those negative things, we have to call them out. We need to continue to listen, to humanize those things that are happening around us, and to understand historical context.”

Dr. Manning reported having no financial disclosures.

Earlier this spring, Kimberly D. Manning, MD, FACP, FAAP, was caring for an elderly Black man with multiple comorbidities at Grady Memorial Hospital in Atlanta, assembling an order for medications and a discharge plan.

“It was very challenging,” Dr. Manning, professor of medicine and associate vice chair of diversity, equity, and inclusion at Emory University, Atlanta, recalled during a May 4 session at SHM Converge, the annual conference of the Society of Hospital Medicine.

At one point, the patient glanced at her, shrugged, and said: “You know, Doc, we get in where we fit in.”

“He was talking about the idea that people who come from historically disadvantaged backgrounds just have to try to figure it out, have to try to make a dollar out of 15 cents,” Dr. Manning said. “This, to me, really underscores what we mean when we say health disparities, this idea that there are people who are working hard and doing the best that they can but who still are forced to ‘get in where they fit in.’”

The Centers for Disease Control and Prevention defines health disparities as preventable differences in the burden of disease, injury, violence, or opportunities to achieve optimal health that are experienced by socially disadvantaged populations. “When we think about health disparities we often think about many diagnoses,” Dr. Manning continued. “We think about HIV and the disparate care and outcomes we’ve seen in populations of individuals who come from minority backgrounds. We see disparities in obesity, cancer, cardiovascular disease, infant mortality and maternal death, hospital readmissions, and COVID-19. We know that people who do not have access to health care or to healthy neighborhoods and environments or who are economically disadvantaged have poorer outcomes. It plays out with all of these diagnoses.”

In her opinion, health disparities in hospital medicine fall into in one of three buckets: diagnosis and triage, hospital stay and treatment, and sticking the landing – “that is, after a patient leaves the hospital,” Dr. Manning explained. “The hospital stay is the turn on the balance beam. You can do everything perfectly, but then you must dismount. To score a ‘10’ you have to stick the landing. That means being able to get your medications, being able to get to and from clinic appointments, being able to understand the directions you’ve been given. All of these things are intertwined, the inpatient and outpatient care.”

The roots of health disparities in hospitalized patients stem from centuries ago, she said, when America’s health care system was built to benefit white male landowners and their families. Health care for Blacks, on the other hand, “was focused on function, almost like veterinary care, or experimentation,” Dr. Manning said. “After slavery ended, many historically Black institutions of higher learning opened, including medical schools. In 1909, there were seven historically Black medical schools. Acknowledging the history that preceded disparities is essential.”

In her view, the path to improving health care disparities starts with conceding that structural racism exists in the practice of medicine. “This means that health disparities are connected to systemic and individual issues, including our biases,” Dr. Manning said. “Our system was built on this idea that there is greater value of one group of people above others. Access to care, physician workforce, and biases are impacted by system design. Health equity and health equality are not the same.”

She also underscored the importance of the social determinants of health, or “those things we need to be healthy,” including economic stability, neighborhood and physical environment, educational opportunities, access to good food, community and social context, and the idea of health care as a human right and understanding our health care system. “This is what is necessary,” she declared. “Without all of these together, we can’t have the health outcomes that we desire.”

As hospital leaders work to build a more diverse physician workforce, Dr. Manning emphasized the importance of forming antiracism policies by addressing questions such as what will we not stand for? How will we protect and create psychologically safe environments? What is our commitment to diversity in leadership and in trainees? What is our commitment to implicit bias training and bystander training?

“We have to get uncomfortable enough to advocate with urgency because all of these are necessary factors to mitigate health disparities,” she said. “Though the systemic issues are the most urgent, on an individual level, we must continue to disrupt the negative ideology and stereotypes that threaten our environment every day. When we see those negative things, we have to call them out. We need to continue to listen, to humanize those things that are happening around us, and to understand historical context.”

Dr. Manning reported having no financial disclosures.